Suzanne R. Pfeffer

Biosketch

Suzanne R. Pfeffer, PhD is the Emma Pfeiffer Merner Professor of Medical Sciences and Professor and former Chairman of the Department of Biochemistry at Stanford University School of Medicine. She earned her AB in Biochemistry from the University of California Berkeley and the PhD in Biochemistry and Biophysics from the University of California at San Francisco (UCSF). She was a postdoctoral fellow at UCSF and then a Helen Hay Whitney Fellow at Stanford University before she joined the Stanford Department of Biochemistry faculty in 1986. She is a fellow of the American Academy of Arts and Sciences, the American Association for the Advancement of Science and the American Society for Cell Biology and a member of the NAS. She has been President of the American Society for Cell Biology and the American Society Biochemistry and Molecular Biology and was a National Science Foundation Presidential Young Investigator; she is currently an Aligning Science Across Parkinson’s Disease Investigator.

Research Interests

Dr. Pfeffer studies the molecular basis of Parkinson’s disease, with a focus on Leucine Rich Repeat Kinase 2 (LRRK2). Activating mutations in LRRK2 are among the most common causes of inherited Parkinson’s, the hallmark of which is death of dopamine neurons in the Substantia nigra. Pfeffer has shown that LRRK2 phosphorylation of a subset of small GTPases called Rab proteins blocks the ability of rare interneurons to provide Hedgohog pathway-activated neuroprotection to dopamine neurons in both mouse and human brains. Her recent work suggests that this represents a convergent mechanism that may explain how other loss of function mutations in genes such as PINK1 or GBA1 lead to Parkinson’s. Pfeffer is also studying the regulation of LRRK2 and has shown that substrate Rab GTPases recruit the kinase to membranes and activate it there. Rab-specific phosphatases control the amount of Rab phosphorylation and both the kinase and phosphatases represent important targets for future therapies; indeed, LRRK2 inhibitors show great promise in restoring Hedgehog signaling and dopaminergic neurite density in mouse PD models.